Auxin, cytokinin and the control of shoot branching

Abstract

Background: It has been known for many decades that auxin inhibits the activation of axillary buds, and hence shoot branching, while cytokinin has the opposite effect. However, the modes of action of these two hormones in branching control is still a matter of debate, and their mechanisms of interaction are equally unresolved.

Scope: Here we review the evidence for various hypotheses that have been put forward to explain how auxin and cytokinin influence axillary bud activity. In particular we discuss the roles of auxin and cytokinin in regulating each other's synthesis, the cell cycle, meristem function and auxin transport, each of which could affect branching. These different mechanisms have implications for the main site of hormone action, ranging from systemic action throughout the plant, to local action at the node or in the bud meristem or leaves. The alternative models have specific predictions, and our increasing understanding of the molecular basis for hormone transport and signalling, cell cycle control and meristem biology is providing new tools to enable these predictions to be tested.

Fig. 1.

Auxin limits CK availability. One proposed model for the regulation of shoot branching by auxin and CK is based on the assumption that CK is a second messenger of auxin. In this model, auxin limits the availability of the antagonistically acting CKs to lateral buds. IPTs in the nodal region of the stem produce CK, which is subsequently transported into the buds to promote bud activation. CK entering lateral buds is proposed to be mainly derived from biosynthesis in stems, but there may be additional relevant sites, e.g. roots. Auxin can repress CK synthesis by inhibition of IPTs, which is dependent on AXR1 function. Thus the amount of auxin in the main stem PATS can regulate bud activity without entering buds. AXR1, AUXIN RESISTANT1; CK, cytokinin; IPT, isopentenyl transferase; PATS, polar auxin transport stream.

Fig. 2.

Bud activation and auxin transport. One model for the mechanism by which auxin regulates bud outgrowth relies on establishment of auxin export out of the bud as a prerequisite to allow bud outgrowth. An initial auxin flow towards an auxin sink promotes auxin transport canalization along this path. The polarization and upregulation of auxin transport feeds back to promote auxin flow further. The canalization of auxin transport into cell files connecting the auxin source (bud) to the auxin sink (main stem) allows sustained auxin export out of the bud. This means that auxin export out of the bud can be prevented if the main stem is a weak auxin sink. This can be achieved by increasing the amount of auxin transported in the PATS in the main stem. Therefore, if CK in the primary apex promotes auxin synthesis and/or PATS, this would inhibit bud outgrowth. On the other hand, if CK promotes auxin synthesis and/or auxin flow in the bud, it would promote bud outgrowth. CK, cytokinin; PATS, polar auxin transport stream.

Fig. 3.

(A) Bud activation and the cell cycle. This model is built on the assumption that CKs regulate TCP transcription factors and those in turn regulate cell cycling to control bud activity. CK entering buds promotes bud activity by suppressing TB1-like genes that restrict cell cycling and negatively regulate bud outgrowth. Other TCP family members have the opposite effect. They promote cell cycling during bud activation, for example by upregulating PCNA. CKs may also promote cell cycling in meristems more directly by inducing cycD transcription. (B) Bud activation and the cell cycle. Another model proposes that auxin export out of the bud is a key regulator that governs bud activity. In this scenario auxin export is a prerequisite for bud activation. It is antagonistically regulated by auxin in the primary stem PATS and by CK, which may enter the bud. Once bud auxin export enables bud activity, the cell cycle machinery gets going, which is in part mediated by TCP transcription factors via PCNA. If lack of auxin export prevents bud outgrowth, this decision is stabilized at least in part by TB1-like genes, which may suppress cell cycling and keep the bud inactive. CK, cytokinin; cycD, cyclinD; PATS, polar auxin transport stream; PCNA, proliferating cell nuclear antigen; TB1-like, Teosinte Branched1-like; TCP, Teosinte branched-Cycloidea-PCF.